CTLA4 and neoplasm: Bioinformatic analyses revealed that through METTL3 and IGF2BP2, circQSOX1 was upregulated and sponged with miR-326 and miR-330-5p to promote PGAM1 expression, which further activated glycolysis and cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) expression, contributing to tumor immune escape [185].